Korean J Anesthesiol.
2023 Dec;76(6):627-639. 10.4097/kja.23323.
Effects of sevoflurane on metalloproteinase and natural killer group 2, member D (NKG2D) ligand expression and natural killer cell-mediated cytotoxicity in breast cancer: an in vitro study
- Affiliations
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- 1Department of Anesthesia and Pain Medicine, Pusan National University School of Medicine, Busan, Korea
- 2Biomedical Research Institute, Pusan National University Hospital, Busan, Korea
- 3Department of Anesthesiology and Pain Medicine, School of Dentistry, Institute for Translational Research in Dentistry, Kyungpook National University, Daegu, Korea
- 4Department of Biochemistry, Pusan National University School of Medicine, Yangsan, Korea
- 5PNU BK21 Plus Biomedical Science Education Center, Pusan National University School of Medicine, Yangsan, Korea
- 6Department of Anesthesiology and Pain Medicine, Kyungpook National University School of Medicine, Daegu, Korea
- 7Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea
- KMID: 2548331
- DOI: http://doi.org/10.4097/kja.23323
Abstract
- Background
We investigated the effects of sevoflurane exposure on the expression of matrix metalloproteinase (MMP), expression and ablation of natural killer group 2, member D (NKG2D) ligands (UL16-binding proteins 1–3 and major histocompatibility complex class I chain-related molecules A/B), and natural killer (NK) cell-mediated cytotoxicity in breast cancer cells.
Methods
Three human breast cancer cell lines (MCF-7, MDA-MB-453, and HCC-70) were incubated with 0 (control), 600 (S6), or 1200 μM (S12) sevoflurane for 4 h. The gene expression of NKG2D ligands and their protein expression on cancer cell surfaces were measured using multiplex polymerase chain reaction (PCR) and flow cytometry, respectively. Protein expression of MMP-1 and -2 and the concentration of soluble NKG2D ligands were analyzed using western blotting and enzyme-linked immunosorbent assays, respectively.
Results
Sevoflurane downregulated the mRNA and protein expression of the NKG2D ligand in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells but did not affect the expression of MMP-1 or -2 or the concentration of soluble NKG2D ligands in the MCF-7, MDA-MB-453, and HCC-70 cells. Sevoflurane attenuated NK cell-mediated cancer cell lysis in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells (P = 0.040, P = 0.040, and P = 0.040, respectively).
Conclusions
Our results demonstrate that sevoflurane exposure attenuates NK cell-mediated cytotoxicity in breast cancer cells in a dose-dependent manner. This could be attributed to a sevoflurane-induced decrease in the transcription of NKG2D ligands rather than sevoflurane-induced changes in MMP expression and their proteolytic activity.
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